PATIENT’S WITH PROBLEMS OF
GAS EXCHANGE
PART TWO
By Linda Self
PULMONARY TUBERCULOSIS
Infectious disease affecting lung parenchyma
 Can be extrapulmonary as well
 Primary causative pathogen is Mycobacterium
tuberculosis
 Sensitive to heat and ultraviolet light
 Estimated to affect one third of the world’s
population
 Cause of death in 11% of those with AIDS
 Anti-TB drugs developed in 1952
 Occurrence gradually decreased until 1985

PULMONARY TUBERCULOSIS
Spreads by airborne transmission including
talking, coughing, sneezing, laughing or singing
 Pathophysiology—bacteria >>airways>>alveoli>>
Immune response>>tissue reaction results in
exudate>>bronchopneumonia 2-10 weeks after
exposure
 Granulomas contain live and dead bacilli, are
surrounded by macrophages>>protective wall,
central portion is called Ghon tubercle
 Ghon tubercle contains cheesy mass, may scar,
bacteria dormant until appropriate conditions

PULMONARY TUBERCULOSIS
Reactivation allows release of cheesy material
into bronchi
 Bacteria then become airborne resulting in
spread of the disease

RISK FACTORS FOR TUBERCULOSIS
Close contact w/someone with TB—duration,
proximity, degree of ventilation
 Immunocompromise
 Substance abuse
 Indigent
 Immigration from countries with high
prevalence—SE Asia, Africa, Latin American,
Caribbean
 Institutionalization
 Living in overcrowded, substandard housing
 Health care workers performing high risk
activities

SIGNS AND SYMPTOMS OF TUBERCULOSIS
Fever
 Cough
 Night sweats
 Fatigue
 Weight loss
 Extrapulmonary much more common in those
with AIDS

ASSESSMENT AND DIAGNOSIS
Mantoux test with PPD—read 48-72 h, assess
erythema and induration
 5mm significant in those at risk (known exposure
and or positive chest xray) or are HIV positive
 10mm significant in those with normal immunity
 BCG effective in 76% who receive it

QUANTIFERON-TB GOLD TEST
2005 FDA approved Gold test
 Is enzyme linked immunosorbent assay (ELISA)
that detect release of interferon-gamma by WBCs
when infected blood is incubated with specific
peptides
 Available in 24h
 Not affected by prior BCG
 Still not widely used

CLASSIFICATION
Class 0—no exposure
 Class 1—exposure, no infection
 Class 2—latent infection; no disease (positive
PPD but no evidence of active TB
 Class 3—disease; clinically active
 Class 4—disease; not clinically active
 Class 5—suspected disease; diagnosis pending

TB AND GERONTOLOGIC CONSIDERATIONS
May be atypical in elderly
 May exhibit unusual behavior and altered mental
status
 May have fever, anorexia and weight loss
 May have delayed or no reaction to tuberculin
skin test

MEDICAL MANAGEMENT
Treated with chemotherapeutic agents for 6-12
months
 Resistance increasing. May be primary,
secondary, or multidrug resistant.
 Primary—resistance to one of first line drugs in
those who have not had prior treatment
 Secondary—resistance to one or more anti-TB
drugs in patients undergoing tx
 Multidrug resistance—resistance to two
agents, INH and rifampin.

FIRST-LINE ANTITUBERCULOSIS
MEDICATIONS
INH—B6, check AST and ALT
 Rifadin (rifampin)—check AST and ALT, orange
secretions
 Mycobutin (rifabutin)—avoid protease inhibitors,
check liver enzymes, plts
 Pyrazinamide—monitor uric acid, AST, ALT
 Myambutol (ethambutol)—optic neuritis, caution
w/renal disease.
 Rifamate (combination INH and rifampin)
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TREATMENT GUIDELINES
Two parts—initial tx phase then a continuation
tx phase
 Initial phase consists of INH, rifampin,
pyrazinamide, and ethambutol, usually for 8
weeks
 Then INH and either rifampin or rifapentine for
four months
 Seven month period of tx for those with cavitary
disease, those with +sputum after two months of
tx, see test
 Considered non-infectious after 2-3 weeks of tx
 Total number of doses of chemotherapy more
accurate than actual duration of treatment

TREATMENT GUIDELINES
INH should be considered for those at risk for
significant disease
 Household members of patients with active
disease
 Pt’s with HIV infection who have PPD with 5 mm
induration or >
 Patients with fibrotic lesions indicative of old TB
and a PPD reaction w/5mm induration or more
 Skin test converters
 Users of IV drugs w/ PPD 10mm or >, foreign
born from high risk country, institutionalized,
high-risk, medically underserved

SIDE EFFECTS OF MEDICATION THERAPY
Take medication on empty stomach or 1h before
meals
 On INH, avoid foods with tyramine and
histamine (tuna, aged cheese, red wine, soy
sauce, yeast extracts)—SE include: HA,
hypotension, palpitations, diaphoresis,
lightheadedness
 Significant drug interations with rifampin

SPREAD OF TUBERCULOSIS
Dissemination to non-pulmonary sites is called
miliary TB
 Usually result of reactivation of dormant
infection in the lung or elsewhere
 Can affect kidneys, liver, meninges, spleen, other
 Can occur rapidly or slowly progressive
 Nurse monitors fever, cognition, renal and liver
function, cough and dyspnea
 Tx same as for pulmonary TB

PLEURAL EFFUSION
Is a collection of fluid in the pleural space
 Usually develops secondary to other diseases
 May be complication of heart failure, TB,
pneumonia, pulmonary infections, CT disease,
nephrotic syndrome, neoplastic tumors
 May be r/t bronchogenic cancer

PLEURAL EFFUSION
Fluid accumulates in pleural space. Normal
amount is 5-15 ml.
 Can be a transudate—filtrate of plasma that
moves across capillary walls. R/T factors affecting
formation and reabsorption of pleural fluid.
Indicates no pleural disease. Often heart failure.
 Exudate—extravasation of fluid. Usually results
from inflammation by bacterial products or
tumors.

CLINCAL MANIFESTATIONS
s/s r/t underlying disease
 Severity r/t size of effusion, speed of formation
and underlying lung disease

ASSESSMENT AND DIAGNOSTIC FINDINGS
Decreased breath sounds and fremitus
 Dull with percussion
 Chest xray, CT and thoracentesis reveal fluid
 Patient lies on affected side, can see air-fluid
levels on chest xray
 Pleural fluid –culture, gram stain, acid-fast,
RBCs and WBCs, chemistry, cytologic analysis
and pH.

MEDICAL MANAGEMENT
Find cause
 Prevent reaccumulation
 Relieve s/s
 Thoracentesis—may be with ultrasound guidance
 May have chemical pleurodesis to prevent
reaccumulation. Instill talc into chest tube, clamp
for 60-90 minutes.
 Malignant pleural effusions-small catheter,
surgical pleurectomy, insertion of
pleuroperitoneal shunt

NURSING MANAGEMENT
Implement medical regimen
 Prepare patient for thoracentesis
 Label specimens
 Prepare chest tube and water seal system
 Monitor drainage
 Pain management
 Education

PULMONARY EDEMA
Abnormal accumulation of fluid in lung tissue,
alveolar space or both
 Pathophysiology—2ndary increased
microvascular pressure from abnormal cardiac
function
 Backup of blood into pulmonary vasculature from
inadequate left ventricular function; increased
microvasc. Pressure and fluid leaks into
interstitium and alveoli
 Other causes—hypervolemia, postpneumonectomy, or following re-expansion of
lung after large pleural effusion evacuated

CLINICAL MANIFESTATIONS
Increasing respiratory distress—central
cyanosis,dyspnea, air hunger
 Anxiety and agitation
 Frothy, blood tinged sputum
 LOC changes
 Crackles in lungs
 Chest xray reveals increased interstitial
markings
 Pulse oximetry falls
 ABG reveals hypoxemia

MANAGEMENT
Treating underlying condition
 Ventricular dysfunction-- inotropes, vasodilators,
intra-aortic balloon pump
 May need ventilator assist
 Morphine one of drugs of choice

ACUTE RESPIRATORY FAILURE
Results when supply of oxygen cannot keep up
with rate of oxygen consumption and carbon
dioxide production at cellular level
 Defined as decrease of arteriolar oxygen tension
less than 50 mm Hg and an increase in arteriolar
carbon dioxide > 50 mm Hg and pH < 7.35
 Can have co-existent acute and chronic
respiratory failure—chronic being COPD or
neuromuscular diseases then superimposed heart
failure, resp. infection, etc.

PATHOPHYSIOLOGY

1.
2.
3.
4.
Four classifications
Decreased respiratory drive—Ex. brainstem
injury, sedation
Dysfunction of the chest wall—Ex. myasthenia
gravis, muscular dystrophy, polio
Dysfunction of the parenchyma—pleural
effusion, hemothorax, pneumothorax,
obstruction
Other—Ex. Post-op combination of anesthesia,
sedatives, analgesics, pain may severely depress
respirations
CLINCAL MANIFESTATIONS
Restlessness
 Fatigue
 Dyspnea
 Air hunger
 Tachycardia
 Increased BP
 LOC changes
 Cyanosis
 diaphoresis

MANAGMENT
Aim is to correct underlying cause
 Nurse assists in intubation
 Ongoing respiratory monitoring
 Prevent complications
 Communication and support
 education

ACUTE RESPIRATORY DISTRESS SYNDROME
Sudden and progressive pulmonary edema,
increasing bilateral infiltrates, hypoxemia
refractory to oxygen supplementation and
reduced lung compliance
 S/S occur in absence of left-sided heart failure
 Most often require mechanical ventilation
 Multicausality
 Mortality rate is 50-60%
 Major cause of death is nonpulmonary multiple
system organ failure, possibly w/sepsis

ETIOLOGIC FACTORS R/T ARDS
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Aspiration
Drug ingestion and overdose
Massive transfusions, cardiopulmonary bypass, DIC
Prolonged inhalation of high %O2, smoke or
corrosives
Metabolic disorders—e.g. pancreatitis
Shock
Trauma
Major surgery
Fat or air embolism
Systemic sepsis
Localized infection
PATHOPHYSIOLOGY
Secondary to an inflammatory trigger, release of
cellular and chemical mediators>>>injury to
alveolar capillary membrane
 Leads to leakage of fluid into alveolar
interstitium causing pulmonary edema, damage
to pneumocytes, microatelectasis
 V/Q mismatch—alveolar collapse r/t
inflammatory infiltrate and surfactant
dysfunction
 Fibrosing alveolitis, “stiff lungs”, creates
shunting
 Severe hypoxemia ensues

CLINICAL MANIFESTATIONS
Rapid onset of dyspnea that usually occurs 12-48
hours after initiating event
 Arterial hypoxemia that does not respond to O2
 Chest xray reveals bilateral infiltrates
resembling cardiogenic pulmonary edema

ASSESSMENT AND DIAGNOSTIC FINDINGS
Presents with intercostal retractions and
crackles
 Based on criteria:
 History of systemic or pulmonary risk factors
 Acute onset of respiratory distress
 Bilateral pulmonary infiltrates
 Absence of left heart failure

MEDICAL MANAGEMENT
ID underlying cause
 Intubation
 Ventilator support
 Circulatory support
 Nutritional support
 PEEP—improves oxygenation by preventing
alveolar collapse; use allows lower FiO2
(sometimes)
 With peep, use low tidal volume
 Hemodynamic monitoring

MANAGEMENT OF THE PATIENT WITH
ARDS
Many therapies under investigation including:
neutrophil inhibitors, pulmonary specific
vasodilators, surfactant replacement therapy,
antisepsis agents (Xigris), antioxidant therapy,
steroids
 Nutritional support ensuring caloric intake of 3545 kcal/kg per day

NURSING MANAGEMENT
Implementing medical plan of care
 May perform prone positioning
 Closely monitor for deteriorating status
 Rest
 Treat anxiety
 Sedatives
 Neuromuscular blocking agents such as Pavulon,
Norcuron (vecuronium), Tracrium (atracurium),
and Zemuron (rocuronium)---requires
continuous close monitoring
 Eye care

PULMONARY EMBOLISM
Obstruction of the pulmonary artery or one of its
branches by a thrombus
 Often associated with trauma, major surgery,
pregnancy, heart failure, age greater than 50,
hypercoagulable states, prolonged immobility

RISK FACTORS FOR PULMONARY EMBOLUS
Venous stasis—prolonged immobilization,
prolonged periods of sitting, varicose veins, spinal
cord injury
 Hypercoagulability-injury, tumor (pancreatic,
gastrointestinal, genitourinary, breast, lung),
increased platelet count (splenectomy,
polycythemia)
 Certain disease states—heart disease, trauma,
postop/postpartum, diabetes mellitus, COPD
 Other—obesity, pregnancy, oral contraceptive
use, constrictive clothing, hx of DVT or PE

PATHOPHYSIOLOGY
Caused by blood clot; other emboli such as air,
fat, amniotic fluid, septic
 Often originate in long veins or pelvis
 Also may originate in atria
 With occlusion, substances are released from clot
resulting in constriction of regional blood vessels
and bronchioles>>>results in increased
pulmonary vascular resistance
 This in turn increases work load of right
heart>>>can result in right heart failure,
decrease in systemic blood pressure and
development of shock

CLINICAL MANIFESTATIONS
s/s dependent on size of thrombus
 Dyspnea
 Tachypnea
 Chest pain possibly imitating angina or MI
 Anxiety, fever, tachycardia, apprehension, cough,
diaphoresis, hemoptysis and syncope

ASSESSMENT AND DIAGNOSTIC FINDINGS
Varied symptoms depending on size of thrombus
and area(s) involved
 Chest xray (excludes other causes)
 ECG (T wave changes may be seen)
 peripheral vascular studies, ABGs, V/Q scans
 Spiral CT
 D-dimer
 Pulmonary angiogram—best method of diagnosis
but may not be feasible

PREVENTION
Leg exercises
 Early ambulation
 Elastic stockings/compression stockings
 Anticoagulants—low dose heparin before surgery
but not in those undergoing major orthopedic
surgery, radical prostatectomy, surgery on the
eye or brain. May use low molecular wt. heparin

MEDICAL AND SURGICAL MANAGEMENT
improve respiratory status—oxygen, other
adjuncts
 Anticoagulation—heparin, maintaining APTT
1.5-2 times normal level; coumadin to maintain
INR 2.0-2.5. Refludan (lepirudin) direct thrombin
inhibitors for those unable to take heparin
 Thrombolytic therapy- Surgical intervention—surgical embolectomy,
patient will be placed on bypass machine, high
intraoperative mortality rate

SURGICAL MANAGEMENT CONT.
Transvenous catheter embolectomy using a
vacuum-cupped catheter
 Pulverizing catheters in conjunction with inferior
vena cava filters
 Transvenous filters—Greenfield or umbrella.
Placed in inferior vena cava. Anticoagulation
continued.

NURSING MANAGEMENT
ID risk factors
 Prevent thrombus formation by ambulating
patients, turning, applying pneumatic stockings,
avoiding prolonged sitting, being vigilant about
central venous catheter removal
 Perform thorough history
 Frequent physical assessment
 Monitoring thrombolytic and anticoagulant tx
 Managing pain
 teaching

CASE STUDIES #1
Mr. Embry is a 63 yo male who underwent colon
resection for polyps three days ago. Today he c/o
SOB, BP dropped to 60/40 and spiked a fever of
101.8. Patient became confused and agitated.
ABGs 7.3—46—22—70. He is emergently
intubated and taken to the ICU.
 In ICU patient is placed on ventilator with
following settings: fiO2 90%, SIMV 6 TV 800ml.
Patient is given fluid bolus of 500ml. Started on
dopamine at 3-5mcg/kg/min. Started on
Vancomycin empirically and Swan-Ganz catheter
is inserted. His PCWP is 12.
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CASE STUDY 1
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Following day patient has BP of 135/70 on
dopamine drip of 7mcg. Has been started on TPN
and is receiving MS for comfort. ABGs are as
follows: 7.35—46.1—HCO3 25—pO2 55. Patient’s
FiO2 is increased from 90 to 100%, tidal volume
is 800mL, SIMV is now 10. PEEP of 5 cm of H2O
is added. Two hours after vent settings ABGs are:
7.42—46.2—28.9—75 .
Now fifth postop day, peep is increased to 10 cm
h20. ABGs are 7.43—46.2—30.5—86.8. Patient
condition continues to improve. Gradually patient
is weaned from ventilator. Ten days postop,
patient is extubated and placed on nasal cannula.
CASE STUDY 1
What is the patient’s condition?
 What was the precipitating insult?
 How is the diagnosis made?
 What are some medical complications associated
with this patient’s diagnosis.
 What lab findings are diagnostic?
 What radiologic findings will be seen?
 What is the principal treatment.
 Name some pharmacologic therapies.
 Why might hemodynamic monitoring be
indicated?

CASE STUDY 2
Sandra Brown is a 35 year female who presents
for an elective cholecystectomy. She is married,
has two children. Is on no medications except
OrthoTricyclen. She has a 10 pack year history of
smoking.
 Her preop data include: BP 140/80, HR 88, RR
22, Temp 97.9, Hgb 15 g/dl, Hct 39%, RBCs 5.1,
WBCs 6000, PT 13.2 sec, PTT 35 sec., normal
ECG, Cxray and UA

CASE STUDY 2
Mrs. Brown tolerated the surgery w/o
complications and was admitted to the step-down
unit. VSS. NG in place. Demerol and Vistaril are
given IM q3-4h prn for pain. Encouraged to get
OOB and sit in chair but tolerates only for 15
min.
 Postop Day 2—VSS but with low grade temp of
100. NG out. Started on clear liquids. Labs wnl
except H&H of 10.8 and 35%. When encouraged
to get OOB, patient refuses as “hurts too much”.

CASE STUDY CONT.
Postop Day 3—patient becomes restless and
apprehensive. C/o SOB, chest pain that worsens
with inspiration and right calf pain. Has crackles
in LLL, labored respirations and diaphoresis.
Right calf is war, tender and erythematous. BP is
now 160/90, HR 124, RR 36 bpm, Temp 100.1.
 Placed on O2 at 4L, MD called, stat ABGs
obtained, 12 lead ECG and chest xray obtained.
 ABGs are 7.52—27—pO2 is 78. Cxray reveals
bibasilar atelectasis, ECG reveals Stach.

CASE STUDY 2

Heparin bolus of 10,000 U is administered. VQ
scan revealed perfusion defects of left lung.
Patient is transferred to ICU.
What is your diagnosis?
Next day respiratory status worsens requiring
intubation. Swan-Ganz catheter is inserted.
CASE STUDY 2
What are risk factors for Mrs. Brown?
 What diagnostic tests may be used in the
diagnosis of PE?
 What are some treatments for treating this
condition?
 How can the nurse prevent this condition?
